Injuries in male professional football: A prospective comparison between individual and team-based exposure registration.

Methodological considerations of football injury epidemiology have only scarcely been described. The aim of this study was to evaluate the inter-rater agreement in injury capture rate and injury categorization for data registered in two different prospective injury surveillance audits studying the same two Norwegian male professional football clubs for two consecutive seasons, 2008-2009. One audit used team-based exposure (TBE) recording and the other individual-based exposure (IBE). The number of injuries recorded and corresponding injury rates (injuries/1000 h exposure) were compared between audits. Cohen's kappa and prevalence-adjusted bias-adjusted kappa (PABAK) coefficients were calculated for injury variables. Of 323 injuries included, the IBE audit captured 318 (overall capture rate 98.5%, training 98.9%, match 97.8%) and the TBE audit 303 injuries (overall capture rate 93.8%, training 91.4%, match 97.1%). Agreement analysis showed kappa and PABAK coefficients regarded as almost perfect (> 0.81) for 8 of 9 injury variables, and substantial (ƙ 0.75) for the variable injury severity. In conclusion, the capture rate for training injuries was slightly higher with IBE recording, and inter-agreement in injury categorization was very high.

Regional differences in injury incidence in European professional football.

The objective of this study was to investigate regional differences in injury incidence in men's professional football in Europe. A nine-season prospective cohort study was carried out between 2001-2002 and 2009-2010 involving 1357 players in 25 teams from nine countries. Teams were categorized into different regions according to the Köppen-Geiger climate classification system. Teams from the northern parts of Europe (n = 20) had higher incidences of injury overall [rate ratio 1.12, 95% confidence interval (CI) 1.06 to 1.20], training injury (rate ratio 1.16, 95% CI 1.05 to 1.27), and severe injury (rate ratio 1.29, 95% CI 1.10 to 1.52), all statistically significant, compared to teams from more southern parts (n = 5). In contrast, the anterior cruciate ligament injury incidence was lower in the northern European teams with a statistically significant difference (rate ratio 0.43, 95% CI 0.25 to 0.77), especially for noncontact anterior cruciate ligament injury (rate ratio 0.19, 95% CI 0.09 to 0.39). In conclusion, this study suggests that there are regional differences in injury incidence of European professional football. However, further studies are needed to identify the underlying causes.

Mechanism of vaccinia virus release and its specific inhibition by N1-isonicotinoyl-N2-3-methyl-4-chlorobenzoylhydrazine.

The release of vaccinia virus from RK-13 cells and its specific inhibition by N(1)-isonicotinoyl-N(2)-3-methyl-4- chlorobenzoylhydrazine (IMCBH) was studied. Intracellular naked vaccinia virus (INV) was wrapped by intracytoplasmic membranes, forming an intracellular double-membraned virion. Wrapped virions migrated to the cell surface, where the outer virion membrane presumably fused with the plasma membrane, releasing virus surrounded by the inner membrane, referred to as extracellular enveloped vaccinia virus (EEV). At no time was there any evidence that vaccinia virus acquired an envelope by budding of naked virus from the cytoplasmic membrane. Naked virus and double-membraned virus each constituted about one-third of intracellular virus at 8 and 12 h postinfection (p.i.). Beginning at 16 h p.i., the proportion of intracellular virus occurring as double-membraned virus steadily decreased to 1% at 24 h while the proportion of naked virus rose to 87%. IMCBH inhibited the formation of the double-membraned virion and the appearance of EEV while not affecting the production of INV. IMCBH had no effect on INV infectivity or polypeptide composition, on vaccinia virus-specified membrane-associated proteins or glycoproteins, or on hemadsorption. The presence of IMCBH until 4 h p.i. did not decrease the amount of EEV at 48 h p.i., whereas less than 10% of the normal 48-h EEV yield was obtained if the drug was present during the first 16 h p.i. Cell cultures infected at very low multiplicities showed a rapid virus dissemination in the absence of the drug, whereas the presence of IMCBH very effectively inhibited this spread. We conclude that vaccinia virus is liberated via a double-membraned intermediate as an enveloped virion and that it is this extracellular enveloped virus that is responsible for dissemination of infection.